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Infection and Immunity > 21 Neisseria - immune system > Flashcards

21 Neisseria - immune system Flashcards

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1
Q

what is neisseria like

A

large genus of Gram-negative bacteria

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2
Q

where is neisseria found

A

Natural inhabitants of the mucous membranes of mammals

Several human commensals inhabiting the mucus membranes

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3
Q

human pathogens - neisseria

A

N. meningitidis

N. gonorrhoea

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4
Q

what causes meningococcal diseases

A

Neisseria meningitidis,

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5
Q

what meningococcal diseases can occur

A

meningococcal sepsis

meningitis

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6
Q

what are meningococcal diseases like

A

while normally a harmless commensal, can cause devastating diseases

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7
Q

what is meningococcal sepsis caused by

A

inappropriate immune response

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8
Q

what causes the characteristic of meningococcal diseases - glass cup

A

capillary networks break down and blood not in circulatory system – why glass test occurs
Glass test – rash doesn’t disappear

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9
Q

carriage of meningococcal diseases

A

normally inhabits the nasopharynx

Colonises up to 50% of individuals within a population

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10
Q

transmission of meningococcal diseases

A

Associated with close contact – transmission

Can be coughing, sneezing, kissing

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11
Q

Meningococcal sepsis symptoms

A

High fever
Rash
Arthritis (achy joints)
Coagulopathy (evident as skin lesions but occurs throughout the body)

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12
Q

coagulopathy effect - meningococcal sepsis

A

bacteria will eventually affect the adrenal glands and adrenal insufficiency quickly leads to death

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13
Q

Meningococcal meningitis symptoms

A 
Severe headaches
Photophobia
High fever
Pain and stiffness of the neck, back, and shoulders
nausea
Rash
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14
Q

post infectious sequelae - meningococcal infection

A

Loss of extremities
Liver or kidney failure
Memory loss

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15
Q

what is a gonococcal infection like

A

may be asymptomatic but ultimately this organism is always a pathogen

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16
Q

symptoms of gonococcal disease

A

urethritis (purulent discharge)

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17
Q

where does gonococcal infections infect

A

mucous membranes of the urogenital tract and nasopharynx

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18
Q

what is the major problems with gonococcal diseases

A

antibiotic resistance

More serious for women – can lead to infertility

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19
Q

how is gonococcal diseases spread

A

usually always sexually transmitted disease – but usually is - Infants can get during birth from infected mother

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20
Q

what gonococcal disease can infant get

A

opthalmia neonatorum

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21
Q

Meningococcal pathogenesis

A

Start in oral pharynx and nasopharynx
Associates with mucosal membrane can get between these cells and get into bloodstream
Cross the blood brain barrier - manipulates endothelial cells that make up blood brain barrier
Organisms can get into cerebrospinal fluid

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22
Q

neisseria meningitidis groups

A

Different serogroups if Neisseria meningitidis – depends on which capsule it makes
Serogroup A
Serogroup B, C, W & Y

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23
Q

what is the capsule controlled by

A

Phase-variable antigen (can be turned on/off)

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24
Q

where are Acapsulate isolates of N. meningitidis often found in

25
when are capsulate isolates found
found in cases of invasive meningococcal disease | Exceptions include individuals with complement deficiencies
26
what is the problem with serogroup B
Serogroup B capsular polysaccharide is identical to molecules found on some neuronal cells Seen as a self-antigen and is thus hypoimmunogenic
27
how does type IV pilus grow
pilE form structure of the pilus – added in the periplasm as added the pilus gets pushed out
28
how does type IV pilus disassemble
pilT protein removes subunits – depolymersises pili and pulls it back in
29
what does pilT require
PilT-dependent twitching motility | PilT is required for pilus retraction and therefore necessary for motility
30
what is TspB
T cell stimulating protein B - potent stimulant of T cells
31
where is TspB
outer membrane protein
32
what encodes TspB
prophage found in most hyperinvasive isolates
33
TspB function
Binds immunoglobulin | Inhibits IgM-mediated activation of the classical complement pathway as binds to Fc not FAB part
34
what does TspB do
Promotes survival in normal human serum
35
what is the matrix composed of that envelopes bacteria aggregates
A matrix composed of TspB, IgG and DNA envelopes aggregates of bacteria
36
what makes fHbp
Produced by most strains of N. meningitidis (not all strains)
37
what is fHbp
OM protein
38
what does fHbp do
binds Factor H onto own surface ‘pretend to be host’ so downregulates complement activity
39
what does factor H do
regulates the Alternative pathway of the complement system
40
what is fHbp important for
survival in human blood, serum and in the presence of antimicrobial peptides
41
Mechanisms that contribute to the resistance of Neisseria meningitidis against complement-mediated killing
- Polysaccharide capsule prevent insertion of MAC - Expression of full length LPS is necessary for complement resistance  - C4BP to PorA - significantly increase the survival of the bacteria in the presence of an active complement system - type IV pilus
42
what makes IgA protease
Produced by a number of mucosal pathogens
43
what does IgA protease do
Cleave IgA1, prominent on mucosal surfaces cuts FAB part from Fc part = ineffective
44
what are the Neisserial IgA proteases virulence-related functions
Cleavage of LAMP1 promotes intracellular survival | Acts as a superantigen - massive cytokine release
45
what is IgA protease
Gram-negatives belongs to a class of secreted proteins called autotransporters
46
Antigenic variation
Expression of antigenically distinct functionally conserved moieties within a clonal population
47
Phase variation
Reversible switching between all-or-none (on/off) expressing phase, resulting in variation in the level of expression of one or more molecules between individual cells of a clonal population
48
phase variation examples
Streisinger model of slipped strand mispairing | Phase variation mediated by transposons
49
Streisinger model of slipped strand mispairing
DNA replication when strands come back together the growing strand can result in addition or removal of one or more repeat units from the daughter duplexes Simple repeats, typically mono-, di- or tetranucleotides, are liable to slipped strand mispairing
50
Streisinger model of slipped strand mispairing - repeats occur in promoter region
can affect the spacing or turn of elements of the promoter (e.g. -10 and -35 regions) and thus the efficiency of the promoter
51
Streisinger model of slipped strand mispairing - repeats occur in ORF
changes in repeat number (where the repeat unit does not contain a whole number of codons) can result in placing the region of the gene downstream of the repeat region in or out of frame
52
Phase variation mediated by transposons
Transposons are DNA elements encoding their own excision and insertion at specific sequences within DNA molecules. Insertion within a gene can disrupt it In most cases transposons do not excise themselves precisely and can not mediate phase variation
53
what can switch off capsule expression
Capsule expression can be switched off by transposition
54
how does transposition switch off capsule expression
Insertion sequences responsible for loss of capsule expression in carriage isolates by insertion into siaA and siaD genes (which are necessary for capule production)
55
Gene conversion in Neisseria meningitidis
Gene conversion responsible for antigenic variation particularly of the pilus pilE – pilus Expressed locus Many pilS loci in genome – S =silent (not expressed) can recombine with pilE = new variants Type IV pilus can take up DNA and can then recombine it
56
how is meningococcal immune evasion is triggered
high temperature
57
what are the 3 independent RNA thermosensors in 5’ region of genes involved in immune evasion
Capsule biosynthesis Factor H-binding protein LOS sialylation
58
what does gonococcal infection elicit
TGF-β-mediated suppression of Th1 and Th2 responses (cell-mediated responses and antibody reponses)
59
what do gonococcal lack
No capsular polysaccharide or fHb – don’t normally see disseminated gonococcal disease is rare

Infection and Immunity (29 decks)

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